兔出血症淋巴－网状器官的病理学动态研究

对人工感染兔出血症病毒的淋巴－网状器官进行组织病理学、超微结构及免疫组织化学的动态研究。结果表明；（１）各淋巴－网状器官出现网状细胞、巨噬细胞及浆细胞反应性增生的免疫应答反应及淋巴细胞损伤性变化，主要表现为淋巴滤泡萎缩、出血及局灶性淋巴细胞或网状细胞的坏死。（２）各淋巴－网状细胞出现程度不同的细胞病理效应（ＣＰＥ），尤以胸腺和圆小囊较明显，初期表现为线粒体肿胀和内质网空泡化，进入濒死期时，表现为淋巴－网状细胞的坏死。（３）该病毒对淋巴－网状细胞有亲嗜性，证明病毒可直接侵害淋巴－网状器官，引起免疫缺陷，从而促使本病的发生。     

兔出血症淋巴—网状器官的病理学动态研究

对人工感染兔出血症病毒的淋巴－网状器官进行组织病理学，超微结构及免疫组织化学的动态研究，结果表明：（１）各淋巴－网状器官出现网状细胞，巨噬细胞及浆细胞反应性增生的免疫应答反应及淋巴细胞损伤性变化，主要表现为淋巴滤泡萎缩，出血及局灶性淋巴细胞或网状细胞的坏死。（２）各淋巴－网状细胞出现程度不同的细胞病理效应，尤以胸腺和圆小囊较明显，初期表现为线粒体肿胀和内质肉空泡化，进入濒死期时，表现为淋巴－网状细     

传染性法氏囊病病毒变异E株对法氏囊淋巴细胞形态及功能的影响

利用透射电镜连续观察了传染性法氏囊病病毒变异株人工感染雏鸡后不同时期法氏囊淋巴细胞的超微结构变化,并对法氏囊内SIgM,SIgG,SIgA3种抗体生成阳性细胞数量和血液中IgM,IgA,IgG抗体水平进行检测。观察结果表明,IBDV感染后法氏囊淋巴细胞出现了严重变性、坏死,表现为核染色质浓缩、碎裂、溶解,线粒体溶解呈空泡样结构,其他细胞器破坏溶解,在法氏囊淋巴细胞、巨噬细胞、网状上皮细胞等细胞的胞浆中可见不同类型和排列方式的病毒粒子。IBDV感染后法氏囊内抗体阳性细胞数量和血清中抗体水平均呈现不同程度的下降,揭示雏鸡机体体液免疫功能严重抑制。     

番鸭肝白点病病理学研究

应用番鸭肝白点病分离毒人工感染1日龄雏番鸭，并对发病鸭的肝，脾、脾、心、肺、肾、胰、法氏囊，胸腺，脑和肠等10种器官组织进行了病理组织学观察，结果表明，试验感染发病鸭特征性病理变化主要为肝脾表面及切面的灰白色坏死点；显微结构变化表现为各器官不同程度变性，细胞溶解坏死及血管扩张充血，病灶区及血管周围淋巴单核细胞明显浸润，免疫器官脾，胸腺和法氏囊淋巴细胞变性坏死，数量明显减少，其特征性显微结构变化主要为肝组织程度不一的脂肪变性和空泡变性，小空泡融合成网眼状大空泡或肝细胞呈现局灶性溶解，并见淋巴单核细胞从病灶的周边逐渐向中心浸润，最后形成细胞性结节，脾脏淋巴细胞坏死，数量减少，网状结缔组织显露。     

禽网状内皮组织增殖病的组织病理学和超微结构的动态变化

一日龄雏鸡腹腔接种禽网状内皮组织增殖病病毒(REV),观察感染后不同时期肝、脾、心、脑、胸腺、腔上囊、腺胃、十二指肠、盲肠、胰腺和性腺等器官组织的肉眼,组织学和超微结构的变化。根据组织病理学和超微结构检查表明:禽网状内皮组织增殖病(RE)的典型病变是实质细胞坏死和网状细胞增生。本病的靶器官主要是肝脏,其次是心、脾、腺胃、腔上囊、胰腺和性腺等。本病增生的网状细胞,通过光镜和电镜观察,能区别于鸡马立克氏病和淋巴性白血病。此外REV可导致雏鸡发生生长抑制和腔上囊萎缩,因此对病畜的增重和其它禽病的免疲预防具有较大的影响。     

呼肠孤病毒B3分离株感染番鸭的病理组织学研究

番鸭呼肠孤病毒B3分离株可经滴鼻、饮水、肌肉和爪垫注射与同居感染1日龄敏感番鸭，潜伏期3－11d，死亡率100％；接种1日龄番鸭、半番鸭和雏鸡抓垫可引起注射部位炎性反应，爪垫和肌肉注射1日龄半番鸭和雏鸡不死亡，病毒感染番鸭主要引起肝、脾、心肌、肾、腔上囊、腺胃、肠粘膜下层等组织局灶性坏死；肝、脑血管周围和肾间质、肺间质、心肌间有淋巴样细胞或／和蚕噬细胞聚集，法氏囊淋巴细胞变性和坏死，电镜观察表明，感染胚肝细胞和脾淋巴细胞胞浆内有大量病毒样颗粒及近核包涵体，感染细胞多核化、空泡化及颗粒化；发现含有病毒样颗粒的凋亡细胞；吞噬细胞胞浆内有病毒样颗粒和含病毒样颗粒的调亡小体，此项研究为国内首次报道。     

IBDV人工感染雏鸡免疫器官病理形态学观察

对雏鸡人工感染传染性法氏囊病毒（IBDV）后,不同阶段免疫器官的病理组织学及超微病理形态学变化作了详细的观察和研究。结果表明,IBDV人工感染雏鸡后,攻击的靶器官是法氏囊,致法氏囊萎缩坏死。同时,对脾脏、胸腺、盲肠扁桃体及哈德尔氏腺等免疫器官组织亦造成一定的损伤。超微病理形态学观察表明,早期各免疫器官内淋巴细胞出现内质网扩张,线粒体肿胀、空泡化,核变形、溶解,淋巴细胞坏死和崩解等变化,并在法氏囊淋巴细胞和巨噬细胞及盲肠扁桃体网状细胞内发现病毒粒子。受损的免疫器官组织能够得到修复     

实验性鸡马立克氏病免疫病理学研究 Ⅲ:中枢免疫器官病理形态学观察

本试验对健康接种京毒—1号MD强毒鸡和免疫后接种MD强毒鸡的中枢免疫器官进行了病理组织学动态观察;并对健康攻毒后30～40天雏鸡的法氏囊进行了组化染色和超微结构的观察。结果表明:实验性鸡马立克氏病时中枢免疫器官的病理组织学变化主要表现为淋巴滤泡或小叶的萎缩、淋巴细胞大量变性、坏死和网状细胞活化增生,法氏囊中还可见到大量腺腔和囊腔的出现及间质中大量带有T淋巴细胞标志的淋巴样细胞的浸润。法氏囊滤泡超徽结构的变化,主要是淋巴细胞的退行性变化,     

幼龄朱鹮新城疫病的病理学观察

对 2例朱　感染新城疫病毒死亡病例进行了系统的病理学观察。结果表明 ,朱　与禽类感染新城疫的病理变化基本一致。眼观所见最显著的病变是腺胃、肌胃粘膜水肿、出血 ,肠道粘膜广泛出血 ,肝肾肿大、出血 ,脑膜充血、出血 ;病理组织学变化为胃、肠道粘膜上皮细胞坏死、脱落 ,固有层毛细血管充血、炎性细胞浸润 ,脑部可见“噬神经”、“卫星化”现象 ,间质毛细血管充血、出血 ;电镜观察发现 ,肝、肾、脑等组织以空泡变性为主 ,细胞中线粒体肿胀 ,内质网扩张 ,核染色质凝集、边移 ,并在肾脏上皮细胞内看到病毒样颗粒。     

幼龄朱新城疫病的病理学观察

对2例朱感染新城疫病毒死亡病例进行了系统的病理学观察.结果表明,朱与禽类感染新城疫的病理变化基本一致.眼观所见最显著的病变是腺胃、肌胃粘膜水肿、出血,肠道粘膜广泛出血,肝肾肿大、出血,脑膜充血、出血;病理组织学变化为胃、肠道粘膜上皮细胞坏死、脱落,固有层毛细血管充血、炎性细胞浸润,脑部可见“噬神经”、“卫星化”现象,间质毛细血管充血、出血;电镜观察发现,肝、肾、脑等组织以空泡变性为主,细胞中线粒体肿胀,内质网扩张,核染色质凝集、边移,并在肾脏上皮细胞内看到病毒样颗粒.     

水稻红莲型粤泰不育花药ATPase超微结构定位

 以ATPase定位研究了红莲型粤泰不育花药和可育花药。结果表明 ,单核中位期可育花粉ATPase定位于覆盖层外侧、柱状层和细胞核 ,单核边位期ATPase定位于覆盖层外侧和细胞核 ;二核期ATPase定位于柱状层、内壁、质膜以及细胞核上 ;三核期ATPase定位于柱状层、内壁、质膜生殖核和营养核的核仁上。单核中位期不育花粉ATPase定位于核仁 ,单核边位期ATPase定位于覆盖层外侧、柱状层、质膜以及细胞核上 ;二核期不育花粉ATPase定位于覆盖层外侧、内壁和核仁。单核中位期可育花药药壁发育良好 ,绒毡层吞噬泡有活跃的ATPase活性 ,单核边位期绒毡层内吞噬泡消失 ,绒毡层内含物减少 ,二核期绒毡层细胞完全解体。单核中位期不育花药药壁发育不良 ,绒毡层内吞噬泡少 ,单核边位期绒毡层出现大量吞噬泡 ,二核期绒毡层存在尚未解体的细胞质和核。大多数不育花药药隔结构及ATPase定位特征与可育花药相似。可能不育花药绒毡层发育迟缓、单核边位期不育花粉细胞质膜活跃的ATPase活性及花粉核异常与花粉败育存在较为密切的关系。     

Glial responses to degenerating cerebellar cortico-nuclear pathways in the cat

Astrocytic changes in regions of long-term, cerebellar corticonuclear degeneration are characterized by large increases in cytoplasmic volume, as well as by formation of vacuoles and fibrils. Lipids are demonstrable in the vacuoles with oil red-O staining.     

疑似鸭新型病毒性传染病在山东的流行情况初步调查及病理学观察

自2010年8月份以来,一种疑似鸭新型病毒病在山东迅速流行,给山东养鸭业造成了巨大损失。为了解本病在山东的流行状况,对临床典型病例临诊症状及剖检病变进行了详细研究,并对其组织器官进行病理组织学观察。结果表明:山东商品蛋鸭、肉种鸭和商品肉鸭均有发病,许多区域的鸭群发病率达100%;流行广、传播快、发病急、发病率高、药物治疗无效、病程长(2～3周)及死淘率(6%～10%)不是很高是该病流行病学的基本特征;临诊主要表现发热、拉稀、采食迅速减少、产蛋严重下降及神经症状;回肠中部黏膜卵圆形肿胀、脾脏灶状坏死、卵泡及输卵管萎缩、肝变性肿胀或出血及心内外膜出血为其主要剖检病变;病理组织学变化主要表现消化道急性卡他性炎症及局部淋巴组织显著增生,心、肝、肾、胰腺变性坏死或出血,脾脏、法氏囊淋巴组织坏死,以及轻度病毒性脑炎。     

Lysosomal stability during phagocytosis of Aspergillus flavus spores by alveolar macrophages of cortisone-treated mice

Control mice and those treated with cortisone were exposed to aerosols of viable spores of Aspergillus flavus. Fifteen to 20 minutes later, animals were killed, and alveolar macrophages were obtained by tracheobronchial lavage. Electron-microscopic examination of these cells revealed that, whereas the lysosomes of control macrophages showed extensive attraction and fusion with the phagocytic membranes surrounding spores, the lysosomes of macrophages from animals treated with cortisone revealed little, if any, interaction. This diminished lysosomal response in forming phagocytic vacuoles may be important in the subsequent development of hyphal bronchopneumonia which frequently, occurs in cortisonetreated mice exposed to spores of A. flavus.     

丙烷脒对番茄灰霉病菌超微结构的影响

    利用电子显微技术研究了丙烷脒(propamidine)对番茄灰霉病菌(Botrytis cinerea Pers.)菌丝形态和细胞结构的影响.研究发现丙烷脒不仅影响菌丝的生长,而且引起菌丝形态和细胞结构一系列的变化.丙烷脒处理番茄灰霉病菌菌丝后,引起病菌菌丝形态和细胞结构的变化主要包括:菌丝分枝增多,并呈不规则的膨大和缢缩,细胞壁出现不规则的加厚,顶端加厚尤其严重,线粒体数目急剧增多且出现不规则的膨大现象,随着处理时间的延长,细胞出现空泡化和电子致密度增加现象.这些细胞学变化特征最终导致菌丝细胞解体死亡.     

Neurovisceral and skeletal GM1-gangliosidosis in dogs with beta-galactosidase deficiency

Beta-galactosidase-deficient siblings in two litters of English springer spaniel puppies showed a progressive neurological impairment, dwarfism, orbital hypertelorism, and dysostosis multiplex. An excess of GM1-ganglioside was found in the brain. Three abnormal oligosaccharides were present in samples of urine, brain, liver, and cartilage. Light microscopy of selected tissue specimens revealed cytoplasmic vacuoles in neurons, circulating blood cells, macrophages, and chondrocytes. Ultrastructural studies demonstrated that these membrane-bound vacuoles were of two types--one containing lamellated membranes and the other, finely granular material. These clinical and pathological findings are similar to those observed in human patients affected by the infantile form of GM1-gangliosidosis.     

Ultrastructural Pathologic Observation on the Gut-Associated Lymphoid Tissues of Sacculus Rotundus of Rabbits Infected with Rabbit Haemorrhagic Disease Virus

Ultrastructural pathological changes in the gut-associated lymphoid tissues of sacculus rotundus(SR) of rabbits infected with rabbit haemorrhagic disease virus (RHDV) were first observed. There were nu-merous holes at the luminal and basement membrane surfaces of the dome epithelium(DE), consistently ac-companied by necrosis of lymphocytes and M-cells, and pronounced depletion of lymphocytes in the domes andfollicles, decrease of DE complex with formation of pseudomembranous structure on the surface of the domeepithelium. A specific finding in lymphocytes and macrophages was that severe destruction detraction of themembrane of rough endoplasmic reticulum(RER) was accompanied by conspicious increase of solitary, ribo-some-like particles in the cytoplasm, with appearances of intranuclear particles and intranuclear inclusions. Itwas found that there were many round and dense virion-like particles, with 26 nm in diameter, in the nucleiand cytoplasm of lymphoctes, plasma cells, macrophages and fibroblasts, or in degenerated cells and cellulardebris. At the same time, another round virion-like particles about 34 nm in diameter were also seen in the cy-toplasm of some cells and interstitium. The results indicated that the appearances of the ribosome-like parti-cles, virion-like particles and inclusion bodies were related to the replication and assembly of RHDV. Thepresent observations suggested that DE of sacculus rotundus could be a open pathway and a transporting routefor the entry of antigens into hosts. While the antigen is profoundly deleterious, DE may be as a closed portalor a barrier preventing the foreign antigenic materials from invading.     

新型H3N8亚型禽流感病毒分离鉴定与鸡致病性研究

为调查我国多个省份鸡群中发生一种以眼睑肿胀出血、呼吸道症状、产蛋鸡产蛋率急性下降为特征的传染性疾病的致病病原,本研究对发病鸡群进行流行病学调查,病原分离鉴定,病毒全基因序列分析,并对分离病毒进行了动物回归试验。结果表明:1)该病自2021年12月首先发现于广东省某三黄鸡群,随后陆续在福建、安徽、江苏、河南等多个省份鸡群中发生,鸡群发病率高,后期易继发感染细菌,死亡率1%~10%;2)实验室初步诊断为H3N8亚型禽流感;3)全基因组序列分析表明,该病毒为新型禽流感病毒,系欧亚禽分支H3基因、北美禽分支N8基因与G57基因型H9N2病毒内部基因组成的三源重排病毒;4)新型H3N8病毒对SPF鸡高度易感,感染鸡表现为眼睑肿胀出血,轻微呼吸道症状;病理变化为哈德氏腺黏膜坏死,鼻甲、气管纤毛上皮细胞坏死,黏膜下层炎性细胞浸润,肺脏支气管肺炎;病毒可通过口咽和泄殖腔排毒,排毒时间为5~7 d;病毒在鼻甲、气管和肺脏中可高效复制,并且可以在哈德氏腺等肺外脏器复制。综上,新型三源重排H3N8禽流感病毒对鸡高度适应,对呼吸系统致病性较强,应尽快开展系统的流行病学监测,及早对病毒的源头及传播途径进行防控,力争将这种新型病毒消灭在流行早期阶段。     

The brain in AIDS: central nervous system HIV-1 infection and AIDS dementia complex

Infection with human immunodeficiency virus type 1 (HIV-1) is frequently complicated in its late stages by the AIDS dementia complex, a neurological syndrome characterized by abnormalities in cognition, motor performance, and behavior. This dementia is due partially or wholly to a direct effect of the virus on the brain rather than to opportunistic infection, but its pathogenesis is not well understood. Productive HIV-1 brain infection is detected only in a subset of patients and is confined largely or exclusively to macrophages, microglia, and derivative multinucleated cells that are formed by virus-induced cell fusion. Absence of cytolytic infection of neurons, oligodentrocytes, and astrocytes has focused attention on the possible role of indirect mechanisms of brain dysfunction related to either virus or cell-coded toxins. Delayed development of the AIDS dementia complex, despite both early exposure of the nervous system to HIV-1 and chronic leptomeningeal infection, indicates that although this virus is "neurotropic," it is relatively nonpathogenic for the brain in the absence of immunosuppression. Within the context of the permissive effect of immunosuppression, genetic changes in HIV-1 may underlie the neuropathological heterogeneity of the AIDS dementia complex and its relatively independent course in relation to the systemic manifestations of AIDS noted in some patients.